The human interleukin-2 (IL-2) receptor has been characterized at the gene, mRNA, and protein levels. The receptor gene contains 8 exons and is located on the short arm of chromosome 10. Transcription of receptor mRNA is initiated at two discrete start sites in normal activated T cells. The 5' flanking region of the receptor gene contains regulatory regions responsive to stimuli which activate IL-2 receptor expression as indicated by linking this region to the chloramphenicol acetyltransferase (CAT) reporter gene. Preliminary data also suggest the presence of an enhancer-like sequence located 5' to the two promoter segments. A secreted form of the IL-2 receptor protein has been produced using an "anchorminus" cDNA construct expressed in mouse L cells. The full-length IL-2 receptor cDNA has also been expressed in human CEM T cells utilizing an amphotropic recombinant retroviral vector. The infected CEM T cells were proven to express both high and low affinity forms of the IL-2 receptor. The mechanism of HTLV-I- and HTLV-II-induced T-cell transformation and accompanying deregulated expression of IL-2 receptors has been explored. Utilizing retroviral vectors, the transactivator (tat) gene of HTLV-II was introduced into Jurkat T cells in both the sense and antisense orientation. These cells were then studied for altered expression of various cellular genes. We observed that the expression of genes encoding the IL-2 receptor, IL-2, and class II major histocompatibility antigens was activated in cells containing the sense tat gene but not in cells containing the antisense tat gene or infected with the control parental retrovirus lacking the tat gene. These data indicate that the transactivator gene of HTLV-I and -II not only augment viral replication but also alter the expression of genes which play a key role in T-cell activation and growth.